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Smarca4 coordinates chromatin accessibility and metabolic programs to sustain hematopoietic stem cell function

GSE318940 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 25 samples Submitted 2026/02/16 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 25 samples

What it is
ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism
Mus musculus (mouse)
Samples
25 samples: 21 distinct titles, 3 of them repeatedGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Hematopoietic stem cells (HSCs) sustain lifelong hematopoiesis by balancing quiescence, self-renewal, and differentiation. However, immunophenotypic definitions of HSCs often fail to capture their functional state, particularly under conditions of stress, aging, or disease, where phenotypic HSCs may accumulate despite profound defects in long-term reconstitution.
Read the full summary ↓
Here, we identify the chromatin remodeling ATPase Smarca4 (BRG1) as a critical regulator of functional HSC integrity. Conditional deletion of Smarca4 in the adult hematopoietic system leads to rapid hematopoietic failure, characterized by an expansion of phenotypically defined HSCs with impaired durable self-renewal capacity. Mechanistically, Smarca4 cooperates with the lineage-associated transcription factor RUNX1 to maintain chromatin accessibility and enhancer activity at the Pparg locus. Loss of Smarca4 selectively disrupts enhancer-associated H3K27ac, rewires metabolic gene programs, and compromises cellular energy homeostasis in HSCs. Restoration of Pparg expression partially rescues metabolic features and early progenitor composition but fails to restore normal differentiation output. Together, our findings establish Smarca4 as an essential epigenetic coordinator that integrates chromatin architecture with metabolic programming to sustain functional hematopoietic stem cell identity.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE318940_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1420855 and SRA study SRP675885. Searching any of these in the dataset finder brings you back here.

Study design
21 distinct titles, 3 of them repeated
Brg1 ×10 ATAC-WT ×4 ATAC-CKO ×3

How we read this: Read from 35 sample titles: 21 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

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